Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to evaluate the clinical diagnostic value of serum total bile acid (STBA) in hepatobiliary diseases. Fasting STBA was measured using the enzymatic colorimetric method in 44 normal control cases and 153 cases of hepatobiliary disease, and then abnormal rates were compared to other conventional liver function tests. These 153 cases of hepatobiliary diseases included acute viral hepatitis (10 cases), chronic persistent hepatitis (32 cases), chronic active hepatitis (16 cases), liver cirrhosis (15 cases), alcoholic hepatitis (11 cases), alcoholic fatty liver (23 cases), alcoholic cirrhosis (17 cases), chronic liver diseases with slight fatty changes (10 cases) and hepatocellular carcinoma (6 cases). Except for 8 cases of acute viral hepatitis, the above cases were verified by liver biopsy. There were also 13 cases of biliary tract diseases. Fasting STBA and other conventional liver function tests were used in the above hepatobiliary diseases during the acute, exacerbated or decompensated stage, and the stable or compensated stage, and their abnormal rates compared. The results of this study revealed that the concentration of STBA is raised in various hepatobiliary diseases, which is related to the degree of hepatic cell injury and the various stages of liver. The concentration of STBA was higher in the acute, exacerbated or decompensated stage than in the convalescent, stable or compensated stage of liver diseases. When the abnormal rates of STBA were compared to other conventional liver function tests, the abnormal rates of STBA were not inferior to r-GT, GOT and GPT, and were more accurate than the other liver function tests.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diagnostic value of serum total bile acid in hepatobiliary diseases]. 275 25

Natural killer (NK) and activated killer (AK) cells appear to be important in immunoregulation, elimination of virus-infected cells and resistance to tumours. NK activity against K 562 and AK activity against FL target cells of peripheral blood mononuclear cells (PBMC) from patients with chronic persistent hepatitis (CPH), chronic active hepatitis (CAH), liver cirrhosis (LC) and hepatocellular carcinoma (HCC) were investigated using 51Cr release assay. Spontaneous NK activity of patients with LC (P less than 0.05) and HCC (P less than 0.001) was decreased when compared to that of controls. The sera and PBMC from patients with low NK activity had no inhibitory effect on the NK activity of normal subjects. Indomethacin treatment significantly enhanced the NK activity of controls (P less than 0.05), whereas the drug did not affect that of patients with low NK activity. The percentages of PBMC that reacted with monoclonal antibodies anti-Leu-7 and anti-Leu-11a were similar in controls and patients. However, a Leu-11a+/Leu-7+ ratio, and NK activity of Leu-11+ and Leu-7+ cell-rich populations were significantly decreased in cirrhotic and HCC patients when compared to controls. Interleukin 2 boosted both NK and AK activities of patients, but to a lesser degree in comparison with those of controls when similarly stimulated. gamma-Interferon also significantly augmented NK and AK activities of patients, but the levels of cytotoxicity were lower in HCC patients (P less than 0.05) than those of controls. These findings suggest that the decreased NK and AK activities in chronic liver disease and HCC are due to an altered subpopulation ratio of NK cells and a functional defect of effector cells.
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PMID:Natural killer and activated killer activities in chronic liver disease and hepatocellular carcinoma: evidence for a decreased lymphokine-induced activity of effector cells. 282 Jun 34

The erythrocyte 2,3-diphosphoglycerate (2,3-DPG) was studied in patients with liver diseases, chronic obstructive pulmonary disease, and in normal subjects. The level of 2,3-DPG in liver diseases occurred in the following increasing order: chronic persistent hepatitis, chronic active hepatitis, liver cirrhosis, and cirrhosis with hepatocellular carcinoma. A significant negative correlation between the 2,3-DPG concentration and serum albumin concentration was found in the liver diseases. The 2,3-DPG level was correlated to the serum concentration of total bile acids and to the arterial blood pH. A negative correlation was found between the arterial blood pH and the serum albumin concentration. The level of 2,3-DPG in hepatocellular carcinoma and/or liver cirrhosis was higher than that in more hypoxic chronic obstructive pulmonary disease. And an increased level of 2,3-DPG was also shown in nonhypoxic patients with liver diseases. These results suggest that the level of erythrocyte 2,3-DPG increases according to the severity of the liver disease, and compared to the level in hypoxic chronic obstructive pulmonary disease, the level of erythrocyte 2,3-DPG is higher in both hepatocellular carcinoma and liver cirrhosis.
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PMID:Erythrocyte 2,3-diphosphoglycerate in liver diseases. 282 16

The livers of 16 woodchucks with naturally acquired chronic infection with woodchuck hepatitis virus were examined both grossly and histologically in 14 biopsy specimens and seven necropsy specimens. Fifteen woodchucks had lesions characteristic of chronic hepatitis; ten of these had chronic active hepatitis, four had chronic persistent hepatitis, and one had cirrhosis with nodular regeneration. In one woodchuck there was massive hepatic necrosis attributed to infection with an unclassified protozoan. Thirteen woodchucks had primary hepatocellular carcinoma. Metastasis to the lung was observed in only one woodchuck. These results were compared to liver lesions in 149 woodchuck hepatitis virus-negative woodchucks. Chronic hepatitis comparable to that associated with woodchuck hepatitis virus infection was not observed in woodchuck hepatitis virus-negative woodchucks although in one, a single, small hepatocellular adenoma was found.
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PMID:Chronic hepatitis and hepatocellular carcinoma associated with persistent woodchuck hepatitis virus infection. 299 74

Antibody to hepatitis B core antigen of immunoglobulin A class was determined in the serum of patients infected with hepatitis B virus by a sandwich-type solid-phase radioimmunoassay with monoclonal antibodies. The antibody, as defined by a sample to normal ratio greater than 2.1, was detected in all of 39 patients with acute hepatitis, with titers varying widely depending on the time of blood sampling. In persons with persistent infection, the antibody was detected in only 2 (4%) of 46 asymptomatic carriers of the virus, contrasting with the positivity in as many as 15 (41%) of 37 patients with chronic persistent hepatitis, in 45 (94%) of 48 patients with chronic active hepatitis, and in 40 (87%) of 46 patients with liver cirrhosis with or without hepatocellular carcinoma. The mean +/- SE titer of antibody in chronic persistent hepatitis (3.8 +/- 0.9) was significantly lower than those in chronic active hepatitis (13.8 +/- 3.2) and cirrhosis with or without carcinoma (25.6 +/- 6.1) (p less than 0.001). Based on the results obtained, the antibody may reflect hepatic injury in the persistent hepatitis B virus infection.
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PMID:Immunoglobulin A antibody against hepatitis B core antigen in the acute and persistent infection with hepatitis B virus. 299 88

Methacetin undergoes rapid O-dealkylation by hepatic microsomal enzyme systems, and the resultant CO2 is present in the expired air. The rate of O-dealkylation of methacetin was assessed by the [13C]methacetin breath test in seven healthy volunteers and 30 patients with histologically proven chronic liver diseases. The 30-min recovery of orally administered [13C]methacetin as 13CO2 in the exhaled air was significantly reduced in patients with chronic aggressive hepatitis and in those with liver cirrhosis but not in patients with chronic persistent hepatitis or healthy controls. Patients with either advanced cirrhosis or hepatocellular carcinoma showed significantly lower values than those with well-compensated cirrhosis. The levels in two patients with late primary biliary cirrhosis were reduced. These results show that the severity of liver damage can be effectively evaluated by [13C]methacetin breath test. In addition, this test is simple, safe, and time efficient.
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PMID:[13C]methacetin breath test for evaluation of liver damage. 303 Jun 79

Serum cathepsin activity and serum level of glycoproteins were determined in patients with chronic liver disorders (cirrhosis, chronic persistent hepatitis, chronic active hepatitis, hepatoma. An increase of cathepsin activity was found in chronic persistent hepatitis and cirrhosis of the liver. Increased level of glycoproteins was observed, the most evident in patients with chronic active hepatitis. An increase of the ratio cathepsin activity/glycoprotein concentration was found in chronic persistent hepatitis, and a decrease of this ratio was observed in chronic active hepatitis.
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PMID:[Serum cathepsin activity in chronic liver diseases]. 303 88

The attempt to divide the large group of chronic HBsAg carriers into "healthy" vs. those with chronic hepatitis of various intensities is sometimes difficult. The major problems are overlap in clinical manifestations, hepatic test results and histologic as well as virologic features. Nevertheless, this separation is not only conceptually important, but may also be useful in patient management, particularly because of the risk of transition to cirrhosis and HCC. Although at least 75% of patients with HCC associated with HBV have cirrhosis, the time point at which the cirrhosis developed is not established, particularly since the vast majority of chronic HBsAg carriers fall into the "healthy" category. Important unanswered questions are, therefore: how often do "healthy" carriers develop cirrhosis and/or HCC, including the time relations between the two? Does the transformation to HCC result from one or several identifiable acute events in the "healthy" carrier (or in mild CPH) or is it a gradual process of progressing chronic hepatitis B in which intercurrent exacerbations may still play a role? Do the quantitative observations as to the relation between persistent HBV infections and HCC in the East apply to Western countries? Our hypothesis concerning pathogenesis is based on pathologic, molecular, clinical and epidemiologic observations and concepts, and is supported by studies of hepadna virus-infected animals. This thesis proposes that integration of HBV DNA into host chromosomes in acute or chronic hepatitis or during the "healthy" carrier state corresponds to an initiation event similar to that described in chemical carcinogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relation of the hepatitis B virus carrier state to hepatocellular carcinoma. 303 25

HBV DNA was measured in the sera of 69 patients with hepatitis B virus infections. Sixteen patients had acute hepatitis B, 24 had chronic active hepatitis (CAH), 6 had chronic persistent hepatitis (CPH), 5 had cirrhosis without CAH and 18 were asymptomatic HBsAg carriers. In patients with acute hepatitis B who recovered, HBV DNA was present in the serum transiently early in the illness. HBV DNA persisted in the serum in the two patients who developed chronic hepatitis. Sera of 23 of 24 patients with CAH were persistently positive for HBV DNA. There was no relationship between the quantity of HBV DNA in the serum and the histological intensity of activity. Thirteen of the 24 patients with CAH had histological evidence of cirrhosis in addition to CAH and HBV DNA was detected in the sera of all 13. The sera of 2 of 6 patients with CPH were positive for HBV DNA. In one it was positive only where there was clinical evidence of reactivation of HBV infection. The other patient subsequently developed CAH. Sera of 5 patients with established HBsAg positive cirrhosis but without evidence of CAH were negative for HBV DNA. Two of these patients had hepatocellular carcinoma. Sera of 18 asymptomatic anti-HBe positive carriers with normal ALT were negative for HBV DNA. HBeAg and HBV DNA were not always found in the serum together. In acute hepatitis 5 patients with HBV DNA in the serum were HBeAg positive, but in 6 patients the sera were HBeAg positive inthe absenceof HBV DNA.
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PMID:Serum HBV-DNA (hepatitis B virus DNA) in acute and chronic hepatitis B infection. 316 50

Liver histologic findings were studied in 18 children who were 4 to 9 years old, and who had been HBsAg carriers since having been infected by their mothers in the perinatal period. All were born to HBeAg-HBsAg carrier mothers; the children were followed periodically from birth. Throughout their entire course, none developed symptoms or signs suggestive of liver disease. All of the 18 children showed mild but definite liver histologic changes: 15 had nonspecific histologic changes, and three had chronic persistent hepatitis. In 13 of 18 children, follow-up aminotransferase activities were abnormal, but none exceeded 100 KU. At the time of biopsy, ALTs on four children were above the upper limit of normal. All children were HBeAg-positive in early infancy, but five lost this antigen and developed antibody during follow-up. The histologic findings in HBeAg-positive children did not differ from those in children with antibody. Perinatal hepatitis B virus infection has been thought to play an important role in chronic liver disease, including hepatocellular carcinoma. This study indicates that some pathologic changes following perinatal infection begin very early.
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PMID:Prospective study of asymptomatic HBsAg carrier children infected in the perinatal period: clinical and liver histologic studies. 335 19


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